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Srinivasan, R.

Publications and source records attributed to Srinivasan, R..

53 records · Page 3Linked to original sources

Perturbation robustness analyses reveal important parameters in variant interpretation pipelines

MotivationGenome sequencing is being used routinely in clinical and research applications, but subsequent variant interpretation pipelines can vary widely. A systematic approach for exploring parameter choices and selection plays an important role in designing robust pipelines for specific clinical applications. ResultsWe present a framework to be applied in scenarios with limited data whereby expert knowledge informs pipeline refinement. Starting from initial reference variant interpretation pipelines with commonly used parameters, we derived pipelines by perturbing the parameters one by one to determine which parameters can yield meaningful changes in a pipelines performance. We updated the reference pipeline by fixing the value of parameters which have small impact on the pipelines performance. Then we conducted new rounds of perturbation as the process converged, yielding a stable pipeline which is robust. We applied the framework for genetic disease prediction in de-identified exomes from a cohort of 138 individuals with rare Mendelian inborn errors of metabolism (IEMs) and systematically explored how perturbing different parameters affected the pipelines sensitivity and specificity. For this application, we perturbed commonly used parameters in variant interpretation pipelines, including choices of genes, variant callers, transcript models, databases of allele frequencies, databases of curated disease variants, and tools for variant impact prediction. Our analyses showed that choice of variant callers, variant impact prediction tools, MAF threshold, and MAF databases can meaningfully alter results from a pipeline. This work informs the development of exome analysis pipelines designed for newborn metabolic disorder screening and suggests the general application of perturbation analysis in genome interpretation pipeline design.

bioinformatics↗

In situ characterization of calcium fluxes in astrocytic mitochondria from the mouse striatum and hippocampus

Astrocytes govern critical aspects of brain function via Ca2+ signals, the majority of which associate with mitochondria. However, little is known with regard to in situ sources, kinetics or mechanisms of Ca2+ influx in astrocytic mitochondria. To address this knowledge gap, we expressed the genetically encoded calcium indicator, GCaMP6f within the mitochondrial matrix of adult mouse astrocytes in the dorsolateral striatum (DLS) and hippocampus (HPC). We found spontaneous Ca2+ events in astrocytic mitochondria with subcellular differences between somatic, branch, and branchlet mitochondria, as well as inter-regional differences between astrocytes in the DLS and HPC. We also found a strong dependency of spontaneous mitochondrial Ca2+ fluxes on endoplasmic reticulum stores, the surprising lack of a major role for the mitochondrial calcium uniporter, MCU, and dual mitochondrial Ca2+ responses with multiple neurotransmitter agonists. Together, our findings provide a foundational understanding of mechanisms for Ca2+ influx in astrocytic mitochondria within disease-relevant brain regions.

neuroscience↗

DNA from dried blood spots yields high quality sequences for exome analysis

BackgroundDNA sequencing of archived dried blood spots (DBS) collected by newborn screening programs constitutes a potential health resource to study newborn disorders and understand genotype-phenotype relationships. However, its essential to verify that sequencing reads from DBS derived DNA are suitable for variant discovery. ResultsWe explored 16 metrics to comprehensively assess the quality of sequencing reads from 180 DBS and 35 whole blood (WB) samples. These metrics were used to assess a) mapping of reads to the reference genome, b) degree of DNA damage, and c) variant calling. Reads from both sets mapped with similar efficiencies, had similar overall DNA damage rates, measured by the mismatch rate with the reference genome, and produced variant calls sets with similar Transition-Transversion ratios. While evaluating single nucleotide changes that may have arisen from DNA damage, we observed that the A>T and T>A changes were more frequent in DNA from DBS than from WB. However, this did not affect the accuracy of variant calling, with DBS samples yielding a comparable count of high quality SNVs and indels in samples with at least 50x coverage. ConclusionsOverall, DBS DNA provided exome sequencing data of sufficient quality for clinical interpretation.

genomics↗

Methylated PP2A stabilizes Gcn4 to enable a methionine-induced anabolic program

Methionine, through S-adenosylmethionine, activates multifaceted growth programs where ribosome biogenesis, carbon metabolism, amino acid and nucleotide biosynthesis are induced. This growth program requires activity of the Gcn4 transcription factor (called ATF4 in mammals), which enables metabolic precursor supply essential for anabolism. Here, we discover how the Gcn4 protein is induced by methionine, despite conditions of high translation and anabolism. This induction mechanism is independent of transcription, as well as the conventional Gcn2/eIF2 mediated increased translation of Gcn4. Instead, when methionine is abundant, Gcn4 ubiqitination and therefore degradation is reduced, due to the decreased phosphorylation of this protein. This Gcn4 stabilization is mediated by the activity of the conserved methyltransferase, Ppm1, which specifically methylates the catalytic subunit of protein phosphatase PP2A when methionine is abundant. This methylation of PP2A shifts the balance of Gcn4 to a dephosphorylated state, which stabilizes the protein. The loss of Ppm1, or PP2A-methylation destabilizes Gcn4 when methionine is abundant, and the Gcn4-dependent anabolic program collapses. These findings reveal a novel signaling and regulatory axis, where methionine directs a conserved methyltransferase Ppm1, via its target phosphatase PP2A, to selectively stabilize Gcn4. Thereby, when methionine is abundant, cells conditionally modify a major phosphatase in order to stabilize a metabolic master-regulator and drive anabolism.

biochemistry↗

Gcn4 (ATF4) drives a methionine-dependent anabolic program by enabling metabolic precursor supply.

Growth and starvation are considered opposite ends of a spectrum. To sustain growth, cells must manage biomolecule supply to balance constructive metabolism with high translation, through coordinated gene expression programs. Global growth programs couple increased ribosomal biogenesis with sufficient carbon metabolism, amino acid and nucleotide biosynthesis, and how this is collectively managed is a fundamental question. Conventionally, the role of the Gcn4/ATF4 transcription factor has been studied only in the context of amino acid starvation. However, high Gcn4/ATF4 has been observed in contexts of rapid cell proliferation, and the specific role of Gcn4 in growth contexts are unclear. Here, using a methionine-induced growth program in yeast, we show that Gcn4/ATF4 is the fulcrum through which metabolic supply dependent sustenance of translation outputs is maintained. Integrating time-matched transcriptome and ChIP-Seq analysis, we decipher genome-wide direct and indirect roles for Gcn4 in this growth program. Genes that enable metabolic precursor biosynthesis indispensably require Gcn4; contrastingly ribosomal genes are partly repressed by Gcn4. Gcn4 directly binds promoter-regions and transcribes a subset of metabolic genes, particularly driving lysine and arginine biosynthesis. Gcn4 also globally represses lys/arg enriched transcripts, which include the translation machinery. The sustained Gcn4 dependent lys/arg supply is required to maintain sufficient translation capacity, by allowing the synthesis of the translation machinery itself. Gcn4 thereby enables metabolic-precursor supply to bolster protein synthesis, and drive a growth program. Thus, we illustrate how growth and starvation outcomes are both controled using the same Gcn4 transcriptional outputs, in entirely distinct contexts.Competing Interest StatementThe authors have declared no competing interest.View Full Text

systems biology↗

Contribution of structural connectivity to MEG functional connectivity

Structural connectivity by axonal fiber bundles provides the backbone for communication between neural populations. Since axonal transmission occurs on a millisecond time scale, measures of M/EEG functional connectivity sensitive to phase synchronization in a frequency band, such as coherence, are expected to reflect structural connectivity. We develop a complex-valued Gaussian Graphical Model (cGGM) of MEG coherence whose edges are constrained by the structural connectome. The cGGMs edge strengths are summarized by partial coherence, a measure of conditional dependence. We made use of the adaptive graphical lasso (AGL) to fit the cGGMs which allows us to perform inference on the hypothesis that the structural connectome is reflected in MEG coherence in a frequency band. In simulations, we demonstrate that the structural connectivitys influence on the cGGM can be inferred using the AGL. Further, we show that fitting the cGGM is superior to alternative methods at recovering the structural connectome. Graphical modeling of MEG coherence is robust to the source localization estimates required to map MEG from sensors to the cortex. Finally, we show how cG-GMs can be used to explore how distinct parts of the structural connectome contribute to MEG coherence in different frequency bands. We think the cGGM is a useful tool that can improve interpretation of MEG coherence by making a direct link to the structural connectome.

neuroscience↗

LRRK2 regulates innate immune responses and neuroinflammation during Mycobacterium tuberculosis infection

Despite many connections between mutations in leucine-rich repeat kinase 2 (LRRK2) and susceptibility to mycobacterial infection, we know little about its function outside of the brain, where it is studied in the context of Parkinsons Disease (PD). Here, we report that LRRK2 controls peripheral macrophages and brain-resident glial cells ability to respond to and express inflammatory molecules. LRRK2 KO macrophages express elevated basal levels of type I interferons, resulting from defective purine metabolism, mitochondrial damage, and engagement of mitochondrial DNA with the cGAS DNA sensing pathway. While LRRK2 KO mice can control Mycobacterium tuberculosis (Mtb) infection, they exhibit exacerbated lung inflammation and altered activation of glial cells in PD-relevant regions of the brain. These results directly implicate LRRK2 in peripheral immunity and support the \"multiple-hit hypothesis\" of neurodegenerative disease, whereby infection coupled with genetic defects in LRRK2 create an immune milieu that alters activation of glial cells and may trigger PD.

immunology↗

Risk taking to obtain reward: gender differences and associations with emotional and depressive symptoms in a nationally representative cohort of UK adolescents.

BackgroundLarge population-based studies of neuropsychological factors that characterize or precede depressive symptoms are rare and we know little about gender differences in these associations.\n\nMethodsThe Millennium Cohort is a representative UK birth cohort of children born between 2000 and 2002. The Cambridge Gambling Task (CGT) was completed at ages 11 (n=12,355) and 14 (n=10,578). Our main exposure was proportion of points gambled, when odds of winning were above chance (risk taking to obtain reward). We also examined how much adolescents adjusted bets as odds of winning increased (risk adjustment). Outcomes were emotional symptoms at age 11 (SDQ) and depressive symptoms at age 14 (sMFQ). We calculated cross-sectional associations, and a longitudinal association from age 11 to 14, using linear regressions before and after adjusting for confounders.\n\nResultsFemales were less risk taking than males (e.g. females bet 9.22, 95% CI 8.65 to 9.80, percentage points lower at age 11). In univariable models there were cross-sectional associations between risk taking and emotional (age 11) or depressive (age 14) symptoms (e.g. at age 14, a 20-percentage point increase in risk taking was associated with a 0.52 reduction in sMFQ points, 95% CI -.71 to -.33). However, cross-sectional associations were explained by gender differences (at age 14 the association adjusted for gender was: .05, 95% CI -.15 to .25). Longitudinally, there was weak evidence of an association between risk taking and depressive symptoms in females only (a 20-point increase in risk taking at age 11 was associated with a reduction of 0.31 sMFQ points at age 14 (95% CI -.60 to -.02).\n\nConclusionsWe found evidence that adolescent females were less likely to take risks than adolescent males. There was no strong evidence of an association between risk taking and emotional and depressive symptoms, after accounting for gender.\n\nAbbreviationsCGT: Millennium Cohort Study (MCS); Cambridge Gambling Task (CGT); Strengths and Difficulties Questionnaire (SDQ); sMFQ: short Mood and Feelings Questionnaire.

epidemiology↗

Reconfigurations within resonating communities of brain regions following TMS reveal different scales of processing

1An overarching goal of neuroscience research is to understand how heterogeneous neuronal ensembles cohere into networks of coordinated activity to support cognition. To investigate how local activity harmonizes with global signals, we measured electroencephalography (EEG) while single pulses of transcranial magnetic stimulation (TMS) perturbed occipital and parietal cortices. We estimate the rapid network reconfigurations in dynamic network communities within specific frequency bands of the EEG, and characterize two distinct features of network reconfiguration, flexibility and allegiance, among spatially distributed neural sources following TMS. Using distance from the stimulation site to infer local and global effects, we find that alpha activity (8-12Hz) reflects concurrent local and global effects on network dynamics. Pair-wise allegiance of brain regions to communities on average increased near the stimulation site, whereas TMS-induced changes to flexibility were generally invariant to distance and stimulation site. In contrast, communities within the beta (13-20Hz) band demonstrated a high level of spatial specificity, particularly within a cluster comprising paracentral areas. Together, these results suggest that focal magnetic neurostimulation to distinct cortical sites can help identify both local and global effects on brain network dynamics, and highlight fundamental differences in the manifestation of network reconfigurations within alpha and beta frequency bands. 2 Author SummaryTMS may be used to probe the causal link between local regional activity and global brain dynamics. Using simultaneous TMS-EEG and dynamic community detection, we introduce what we call "resonating clusters", or frequency band-specific communities in the brain, as a way to index local and global processing. These resonating clusters within the alpha and beta bands brain display both global (or integrating) behavior and local specificity, highlighting fundamental differences in the manifestation of network reconfigurations.

neuroscience↗

Old fibroblasts secrete inflammatory cytokines that drive variability in reprogramming efficiency and may affect wound healing between old individuals

Age-associated chronic inflammation (inflammaging) has emerged as a central hallmark of aging1-3, but its impact on specific cells is still largely unknown. Fibroblasts are present in all tissues and contribute to wound healing4-6. They are also the cell type that is mostly used for induced pluripotent stem cell (iPSC) reprogramming7 - a process that has implications for regenerative medicine and rejuvenation strategies8-17. Here we show that primary fibroblasts from old mice secrete inflammatory cytokines and that there is an increased variability in reprogramming efficiency between fibroblast cultures from old individuals. Individual-to-individual variability is emerging as a key feature of old age18-21, which could reflect distinct aging trajectories, but the underlying causes remain unknown. To identify drivers of this variability, we perform a multi-omic assessment of young and old fibroblast cultures with different reprogramming efficiency. This approach, coupled with single cell transcriptomics, reveals that old fibroblast cultures are heterogeneous and show a greater proportion of activated fibroblasts that secrete inflammatory cytokines, which correlates with reprogramming efficiency. We experimentally validate that activated fibroblasts express inflammatory cytokines in vivo and that their presence is linked to enhanced reprogramming efficiency in culture. Conditioned-media swapping experiments show that extrinsic factors secreted by activated fibroblasts are more critical than intrinsic factors for the individual-to-individual variability in reprogramming efficiency, and we identify TNF as a key inflammatory cytokine underlying this variability. Interestingly, old mice also exhibit variability in wound healing efficiency in vivo and old wounds show an increased subpopulation of activated fibroblasts with a unique TNF signature. Our study shows that a switch in fibroblast composition, and the ratio of inflammatory cytokines they secrete, drives variability in reprogramming in vitro and may influence wound healing in vivo. These findings could help identify personalized strategies to improve iPSC generation and wound healing in older individuals.

cell biology↗

Network Structure During Encoding Predicts Working Memory Performance

Working memory operates through networks that integrate distributed modular brain activity. We characterize the structure of networks in different electroencephalographic frequency bands while individuals perform a working memory task. The objective was to identify network properties that support working memory function during the encoding, maintenance, and retrieval of memory. In each EEG frequency band, we estimated a complex-valued Gaussian graphical model to characterize the structure of brain networks using measures from graph theory. Critically, the structural characteristics of brain networks that facilitate performance are all established during encoding, suggesting that they reflect the effect of attention on the quality of the representation in working memory. Segregation of networks in the alpha and beta bands during encoding increased with accuracy. In the theta band, greater integration of functional clusters involving the temporal lobe with other cortical areas predicted faster response time, starting in the encoding interval and persisting throughout the task, indicating that functional clustering facilitates rapid memory manipulation.

neuroscience↗

Multi-Scale Neural Sources of EEG: Genuine, Equivalent, and Representative

A biophysical framework needed to interpret electrophysiological data recorded at multiple spatial scales of brain tissue is developed. Micro current sources at membrane surfaces produce local field potentials (LFP), electrocorticography (ECoG), and electroencephalography (EEG). We categorize multi-scale sources as genuine, equivalent, or representative. Genuine sources occur at the micro scale of cell surfaces. Equivalent sources provide identical experimental outcomes over a range of scales and applications. In contrast, each representative source distribution is just one of many possible source distributions that yield similar experimental outcomes. Macro sources (\"dipoles\") may be defined at the macrocolumn (mm) scale and depend on several features of the micro sources--magnitudes, micro synchrony within columns, and distribution through the cortical depths. These micro source properties are determined by brain dynamics and the columnar structure of cortical tissue. The number of representative sources underlying EEG data depends on the spatial scale of neural tissue under study. EEG inverse solutions (e.g. dipole localization) and high resolution estimates (e.g. Laplacian, dura imaging) have both strengths and limitations that depend on experimental conditions. The proposed theoretical framework informs studies of EEG source localization, source characterization, and low passes filtering. It also facilitates interpretations of brain dynamics and cognition, including measures of synchrony, functional connections between cortical locations, and other aspects of brain complexity.

neuroscience↗

Timing of readiness potentials reflect a decision-making process in the human brain

Decision-making in two-alternative forced choice tasks has several underlying components including stimulus encoding, perceptual categorization, response selection, and response execution. Sequential sampling models of decision-making are based on an evidence accumulation process to a decision boundary. Animal and human studies have focused on perceptual categorization and provide evidence linking brain signals in parietal cortex to the evidence accumulation process. In this exploratory study, we use a task where the dominant contribution to response time is response selection and model the response time data with the drift-diffusion model. EEG measurement during the task show that the Readiness Potential (RP) recorded over motor areas has timing consistent with the evidence accumulation process. The duration of the RP predicts decision-making time, the duration of evidence accumulation, suggesting that the RP partly reflects an evidence accumulation process for response selection in the motor system. Thus, evidence accumulation may be a neural implementation of decision-making processes in both perceptual and motor systems. The contributions of perceptual categorization and response selection to evidence accumulation processes in decision-making tasks can be potentially evaluated by examining the timing of perceptual and motor EEG signals.

neuroscience↗

Visual encoding signals around 200 milliseconds track onset of evidence accumulation during human decision making

Encoding of a sensory stimulus is believed to be the first step in perceptual decision making. Previous research has shown that electrical signals recorded from the human brain track evidence accumulation during perceptual decision making (Gold and Shadlen, 2007; OConnell et al., 2012; Philiastides et al., 2014). In this study we directly tested the hypothesis that the latency of the N200 recorded by EEG (a negative peak occurring between 150 and 275 ms after stimulus presentation in human participants) reflects the visual encoding time (VET) required for completion of figure-ground segregation before evidence accumulation. We show that N200 latencies vary across individuals, are modulated by external visual noise, and increase response time by x milliseconds when they increase by x milliseconds, reflecting a linear regression slope of 1. Simulations of cognitive decision-making theory show that variation in human response times not related to evidence accumulation (including VET) are tracked by the fastest response times. A relationship with a slope of 1 between N200 latencies and VET was found by fitting a linear model between trial-averaged N200 latencies and the 10th percentiles of response times. A slope of 1 was also found between single-trial N200 latencies and response times. Fitting a novel neuro-cognitive model of decision-making also yielded a slope of 1 between N200 latency and non-decision time in multiple visual noise conditions, indicating that N200 latencies track the completion of visual encoding and the onset of evidence accumulation. The N200 waveforms were localized to the cortical surface at distributed temporal and extrastriate locations, consistent with a distributed network engaged in figure-ground segregation of the target stimulus.\n\nSignificance StatementEncoding of a sensory stimulus is believed to be the first step in perceptual decision making. In this study, we report evidence that visual evoked potentials (EPs) around 200 ms after stimulus presentation track the time of visual figure-ground segregation before the onset of evidence accumulation during decision making. These EP latencies vary across individuals, are modulated by external visual noise, and increase response time by x milliseconds when they increase by x milliseconds. Hierarchical Bayesian model-fitting was also used to relate these EPs to a specific cognitive parameter that tracks time related to visual encoding in a decision-making model of response time. This work adds to the growing literature that suggests that EEG signals can track the component cognitive processes of decision making.

neuroscience↗

Methionine coordinates a hierarchically organized anabolic program through GCN4

Methionine availability during overall amino acid limitation metabolically reprograms cells to support proliferation, the underlying basis for which remains unclear. Here, we construct the organization of this methionine mediated anabolic program, using yeast. Combining comparative transcriptome analysis, biochemical and metabolic flux based approaches, we discover that methionine rewires overall metabolic outputs by increasing the activity of three key regulatory nodes. These are: the pentose phosphate pathway coupled with reductive biosynthesis, and overall transamination capacity, including the synthesis of glutamate/glutamine. These provides the cofactors or substrates that enhance subsequent rate-limiting reactions in the synthesis of costly amino acids, and nucleotides, which are also induced in a methionine dependent manner. This thereby results in a biochemical cascade establishing an overall anabolic program. For this methionine mediated anabolic program leading to proliferation, cells co-opt a \"starvation stress response\" regulator, Gcn4p. Collectively, our data suggest a hierarchical metabolic framework explaining how methionine mediates an anabolic switch.

systems biology↗

FOXS1 is a Master Regulator of Pathological Epithelial to Mesenchymal Transition in Human Epithelia

Epithelial to mesenchymal transition (EMT) is a biological process involved in normal tissue morphogenesis and also in disease pathology. It causes dramatic alterations in cell morphology, migration, proliferation, and phenotype. We captured the global transcriptional and epigenetic programs elicited when polarized, cobblestone human retinal pigment epithelial (RPE) cells were stimulated to undergo EMT, a process associated with several retinal pathologies. The reorganization of chromatin landscapes occurred preferentially at distal enhancers, rather than promoter regions, accompanied by 3136 significantly changing genes. Of the 95 significantly changing transcription factors, FOXS1 was most upregulated. Loss and gain of function experiments demonstrated that FOXS1 is upstream of canonical EMT regulators, and can stimulate EMT in RPE and other epithelia. Inhibition of p38, stimulated by combined action of the EMT-inducing factors, TGF{beta}1 and TNF, dampened FOXS1 expression. An increase of FOXS1 in several cancers indicates it has a role in several EMT-involved pathologies.

cell biology↗

Sequence Alignment On Directed Graphs

Genomic variations in a reference collection are naturally represented as genome variation graphs. Such graphs encode common subsequences as vertices and the variations are captured using additional vertices and directed edges. The resulting graphs are directed graphs possibly with cycles. Existing algorithms for aligning sequences on such graphs make use of partial order alignment (POA) techniques that work on directed acyclic graphs (DAG). For this, acyclic extensions of the input graphs are first constructed through expensive loop unrolling steps (DAGification). Also, such graph extensions could have considerable blow up in their size and in the worst case the blow up factor is proportional to the input sequence length. We provide a novel alignment algorithm V-ALIGN that aligns the input sequence directly on the input graph while avoiding such expensive DAGification steps. V-ALIGN is based on a novel dynamic programming formulation that allows gapped alignment directly on the input graph. It supports affine and linear gaps. We also propose refinements to V-ALIGN for better performance in practice. In this, the time to fill the DP table has linear dependence on the sizes of the sequence, the graph and its feedback vertex set. We perform experiments to compare against the POA based alignment. For aligning short sequences, standard approaches restrict the expensive gapped alignment to small filtered subgraphs having high similarity to the input sequence. In such cases, the performance of V-ALIGN for gapped alignment on the filtered subgraph depends on the subgraph sizes.

genomics↗